ArticleJournal of the American Society of Nephrology : JASN2008
GDF15 triggers homeostatic proliferation of acid-secreting collecting duct cells.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 80 citations in OpenAlex.
- Roles of GDF-15 in Acute Heart Failure: from Mechanistic Insights to Clinical Applications.International journal of medical sciences · 2026Review
- Novel Roles of GDF15 in Alleviating Renal Fibrosis: Promoting Autophagy and Lysosome Biogenesis via Inhibition of the PI3K/Akt/mTOR Pathway.Journal of cellular and molecular medicine · 2026Article
- GDF-15 and uEGF Independently Associate With CKD Progression in Children.Kidney international reports · 2025Article
- GDF15, an Emerging Player in Renal Physiology and Pathophysiology.International journal of molecular sciences · 2024Review
- Stress-responsive Gdf15 counteracts renointestinal toxicity via autophagic and microbiota reprogramming.Communications biology · 2023Article
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- Mechanistic insights into the primary and secondary alterations of renal ion and water transport in the distal nephron.Journal of internal medicine · 2023Review
- Renal KFrontiers in physiology · 2023Review
- The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosis.American journal of physiology. Renal physiology · 2023Article
- Physiological relevance of proton-activated GPCRs.Pflugers Archiv : European journal of physiology · 2022Review
- Growth Differentiation Factor 15 Protects SH-SY5Y Cells From Rotenone-Induced Toxicity by Suppressing Mitochondrial Apoptosis.Frontiers in aging neuroscience · 2022Article
- Elevated circulating growth differentiation factor 15 is related to decreased heart rate variability in chronic kidney disease patients.Renal failure · 2021Observational
- Growth differentiation factor-15 and incident chronic kidney disease: a population-based cohort study.BMC nephrology · 2021Article
- GDF-15 Predicts In-Hospital Mortality of Critically Ill Patients with Acute Kidney Injury Requiring Continuous Renal Replacement Therapy: A Multicenter Prospective Study.Journal of clinical medicine · 2021Article
- The Clinical Value of GDF15 and Its Prospective Mechanism in Sepsis.Frontiers in immunology · 2021Article
- Adaptive response of the murine collecting duct to alkali loading.Pflugers Archiv : European journal of physiology · 2020Article
- GDF15: A Hormone Conveying Somatic Distress to the Brain.Endocrine reviews · 2020Review
- Renoprotective and Immunomodulatory Effects of GDF15 following AKI Invoked by Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2020Article
- Growth Differentiation Factor 15 in Children with Chronic Kidney Disease and after Renal Transplantation.Disease markers · 2020Article
- GDF-15 in Pulmonary and Critical Care Medicine.American journal of respiratory cell and molecular biology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although adult kidney cells are quiescent, enlargement of specific populations of epithelial cells occurs during repair and adaptive processes. A prerequisite to the development of regenerative therapeutics is to identify the mechanisms and factors that control the size of specific populations of renal cells. Unfortunately, in most cases, it is unknown whether the growth of cell populations results from transdifferentiation or proliferation and whether proliferating cells derive from epithelial cells or from circulating or resident progenitors. In this study, the mechanisms underlying the enlargement of the acid-secreting cell population in the mouse kidney collecting duct in response to metabolic acidosis was investigated. Acidosis led to two phases of proliferation that preferentially affected the acid-secreting cells of the outer medullary collecting duct. All proliferating cells displayed polarized expression of functional markers. The first phase of proliferation, which started within 24 h and peaked at day 3, was dependent on the overexpression of growth differentiation factor 15 (GDF15) and cyclin D1 and was abolished when phosphatidylinositol-3 kinase and mammalian target of rapamycin were inhibited. During this phase, cells mostly divided along the tubular axis, contributing to tubule lengthening. The second phase of proliferation was independent of GDF15 but was associated with induction of cyclin D3. During this phase, cells divided transversely. In summary, acid-secreting cells proliferate as the collecting duct adapts to metabolic acidosis, and GDF15 seems to be an important determinant of collecting duct lengthening.
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